In our society, facial expression is an essential factor of verbal and nonverbal communication. Thus, aging facial muscles can interfere with social and professional success. Aging in the facial region typically means a loss of muscle tone, muscle volume and/or a loss or reduction of connective and fat tissue, e.g., below the eyes and/or at the cheek. As a result of the aging muscles, facial muscles and/or other facial tissues may diminish or atrophy.
There are many problems commonly associated with aging facial muscles. For example, the aging facial muscles can lead people to perceive a person as “old” or “infirm” even though their mental capacity remains intact. In addition, some facial muscle problems that people ascribe to aging, or even to their natural genetic makeup, may be caused or aggravated by other medical problems. It is not surprising that when exercises and medications alone do not provide sufficient improvement, many patients elect more invasive and irreversible surgery, such as face lifts, in an attempt to improve their facial appearance. Even with these consequences, rehabilitation of facial nerves due to aging remains unsatisfactory.
There are also other problems related to dysfunctional facial muscles that can affect a patient's quality of life. Dysfunctional muscles include muscles that do not receive nerve innervation (e.g., due to nerve damage or paralysis), or that do not otherwise fully get stimulated by the nerve for some reason (e.g., synkinetic reinervated muscles). For example, with facial paresis, patients feel stigmatized and often retreat from the public and develop secondary psychological disorders, e.g., depressions. Thus, the patients' quality of life is significantly curbed. Persistent defects after healing are even observed in cases of spontaneous regeneration or optimal and extensive surgical reconstruction of the nerve in cases of nerve transsection and bridging of the defect with neural transplants. Sprouting of the regenerating axons is observed at the site of the lesion even after reconstruction of nerve continuity. At the same time, Wallerian degeneration of the entire affected section of the nerve as far as the muscles is completed until only the Bungner's bands remain as Schwann cell conducting structures. The regenerating neurons with their sprouting axons grow accidentally into these bands of the individual nerve branches and are directed to the peripheral mimic muscles. Individual axons perish and do not reach the periphery, some accidentally reach their original target muscle, while others reach a completely different target muscle. Due to axonal collateral sprouting, the most frequently observed effect is simultaneous sprouting to several target muscles, such as shown in FIGS. 1A and 1B.
As shown in FIG. 1A, normally exactly one axon 2 projects to one end-plate on the muscle fiber 4. Each of the different muscle groups 6 of the face is activated by the motor neuron pool of a subnucleus of the nucleus. As shown in FIG. 1B, despite transsection and optimal reconstruction of the facial nerve, the regenerating axons 2 may sprout collaterally at the site of the lesion. The axons 2 sprout purely accidentally to any muscle fibers 4. Somatotopic order is lost. This leads clinically to simultaneous movement of several target muscles (a condition called synkinesis). Patients often complain about involuntary lid closure while moving the mouth, e.g., when eating. Simultaneous movement of antagonist muscles leads to the autoparalytic syndrome: muscle forces cancel each other out and no movement is observed clinically despite innervation.
New research shows that not only collateral sprouting but also terminal sprouting of the regenerating axons directly at the neuromuscular end-plates causes uncoordinated muscle function, such as shown in FIGS. 2A and 2B. As shown in FIG. 2A, normally exactly one axon 2 projects to one end-plate on the muscle fiber 4. After transsection and surgical reconstruction, however, terminal sprouting may occur (such as shown in FIG. 2B) in addition to collateral sprouting. In this case, individual end-plates may be activated by several axons 2. Thus, in subjects with these kinds of problems, activating a desired facial muscle may entail considerable challenges since stimulating a nerve branch on the damaged side of the subject's face may not activate the corresponding facial muscle, but an entirely different, unpredictable facial muscle or muscles. This explains why the patients' quality of life is significantly limited even after surgical reconstruction of the nerve. If the lesion is so extensive that the remaining peripheral part of the facial nerve is insufficient, or if Bungner's bands are fibrosed due to failed reinnervation and muscles are atrophied due to long-term denervation of more than 3 to 5 years, the patient can no longer be offered a nerve graft.
Possible therapies include dynamic muscle grafts, free nerve-muscle transplantation, implantation of upper lid weights or static suspensions. Functional results of these secondary procedures are even less satisfactory than the above mentioned nerve grafts. These procedures may, at best, restore muscle tone, but facial expression remains very mask-like and the dynamic muscle suspensions allow reproducing only few and very mechanistic movement vectors.